MULTI-MINERAL PLUS ALFALFA

Indications

• Hyperlipidemia
• Digestive disorders
• Nutritional supplementation
• Menopausal symptoms
• Diabetes management

Dosage

Adults: Dosage varies widely based on the form of alfalfa (e.g., capsules, tablets, or sprouts) and individual health needs. It is advised to refer to specific product guidelines or consult a healthcare professional for appropriate dosing.

Mechanism of action

The mechanisms of action of alfalfa are primarily attributed to its phytochemical constituents, including saponins, flavonoids, and coumarins. These compounds may help to lower cholesterol levels by binding bile acids, promoting their excretion, and thereby reducing lipid absorption. Alfalfa also exhibits antioxidant properties, which may help in reducing oxidative stress and inflammation in the body. Additionally, the high fiber content aids in digestive health by promoting bowel regularity.

Pharmacodynamics

Alfalfa has been shown to have various pharmacodynamic effects, including lipid-lowering activity, anti-inflammatory effects, and antioxidant properties. Its saponins can influence lipid metabolism, while flavonoids may exert anti-inflammatory actions. The plant's high fiber content helps to regulate bowel movements and can promote satiety, which may assist in weight management. The bioactive compounds in alfalfa also contribute to its potential benefits in promoting cardiovascular health.

Pharmacokinetics

The pharmacokinetics of alfalfa are not extensively studied; however, it is noted that the bioactive compounds are absorbed through the gastrointestinal tract. The presence of dietary fiber may slow down the absorption of some nutrients, but this can also contribute to overall health benefits. Metabolism of alfalfa constituents occurs mainly in the liver, and excretion primarily happens through feces and urine. The half-life of specific compounds within alfalfa is not well defined.

Adverse effects

• Allergic reactions
• Gastrointestinal upset
• Hypersensitivity reactions

Interactions

• May interact with anticoagulants and antiplatelet medications due to potential vitamin K content
• Can affect the absorption of certain medications due to high fiber content

Precautions

• Use with caution in individuals with hormone-sensitive conditions due to phytoestrogen content
• Monitor for allergic reactions in sensitive individuals

Pregnancy

Consult healthcare professionals before use due to insufficient evidence on safety.

Breast-feeding

Consult healthcare professionals before use as safety is not well established.

Storage

Store in a cool, dry place, protected from light.

Formulations

• Dried leaf powder
• Tablets
• Capsules
• Tinctures

Mechanism of action

Carbonate ions participate in buffering reactions that help maintain pH homeostasis in biological systems. They can react with acids to form bicarbonate and carbon dioxide, thus neutralizing excess acidity in the body. This mechanism is crucial in processes such as respiration and metabolism.

Pharmacodynamics

As a buffer, carbonate helps to stabilize pH levels in different biological environments, preventing excessive acidity or alkalinity that could impair cellular functions. It is involved in the transport of carbon dioxide in the blood and plays a role in maintaining the acid-base equilibrium necessary for physiological processes.

Pharmacokinetics

Carbonate ions are readily absorbed in the gastrointestinal tract when ingested and can be found in various body fluids. They are involved in the bicarbonate buffering system, where they are converted to bicarbonate (HCO3-) and carbon dioxide (CO2) through reactions with acids. The kidneys regulate the levels of bicarbonate and carbonate in the body, excreting or reabsorbing them as needed to maintain homeostasis.

Pregnancy

There is no specific information available regarding the use of carbonate compounds during pregnancy. Consult a healthcare provider for advice.

Breast-feeding

There is no specific information available regarding the use of carbonate compounds while breastfeeding. Consult a healthcare provider for advice.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Copper deficiency
• Menkes disease
• Wilson's disease (as part of chelation therapy)
• Anemia
• Bone health support

Dosage

Children: Refer to established guidelines and clinical protocols for specific copper supplementation or treatment dosages in children, as they vary based on age and clinical condition.

Adults: Refer to established guidelines and clinical protocols for specific copper supplementation or treatment dosages, as they vary based on the condition being treated.

Mechanism of action

Copper exerts its effects primarily through its role as a cofactor for several key enzymes, including cytochrome c oxidase, superoxide dismutase, and ceruloplasmin. These enzymes are crucial for energy production, free radical detoxification, and iron transport, respectively. Copper's involvement in these enzymatic pathways is essential for maintaining cellular homeostasis and overall metabolic function.

Pharmacodynamics

Copper is absorbed in the gastrointestinal tract and is distributed throughout the body, primarily in the liver, brain, heart, and kidneys. It participates in various biochemical processes, such as collagen synthesis and the formation of melanin. The body tightly regulates copper levels to prevent toxicity, as excessive copper can lead to oxidative stress and cell damage.

Pharmacokinetics

Copper is absorbed mainly in the jejunum and ileum of the small intestine, with absorption rates varying based on dietary intake and the presence of other minerals. Once absorbed, copper is transported in the bloodstream bound to plasma proteins, particularly albumin and ceruloplasmin. The liver plays a central role in copper homeostasis, regulating its excretion through bile. The elimination half-life of copper is variable but generally involves continuous turnover within the body, with excess copper being excreted primarily via the biliary route.

Pregnancy

Copper supplements should only be used during pregnancy if the potential benefit justifies the potential risk to the fetus. Consult a healthcare provider before use.

Breast-feeding

Copper is excreted in breast milk, and supplementation should be approached with caution. Consult a healthcare provider for advice.

Storage

Store in a cool, dry place, away from direct sunlight. Keep out of reach of children.

Indications

• Copper deficiency
• Occipital Horn Syndrome
• Menke's disease
• Contraception (via copper IUD)

Dosage

Children: Refer to the BNF for Children for specific dosing information.

Adults: Refer to the relevant clinical guidelines and BNF for specific dosing information.

Mechanism of action

Copper is absorbed from the gastrointestinal tract via high affinity copper uptake proteins and low affinity copper uptake proteins, likely being reduced to the Cu1+ form prior to transport. Inside enterocytes, it binds to the copper transport protein ATOX1, which facilitates its transport to copper transporting ATPase-1 on the Golgi membrane for incorporation into the Golgi apparatus. Once in systemic circulation, copper binds primarily to ceruloplasmin, albumin, and alpha 2-macroglobulin. It acts as a cofactor in a variety of oxidase enzymes and also influences sperm motility when released from copper IUDs, contributing to its contraceptive effect.

Pharmacodynamics

Copper is essential for the activity of many enzymes and plays a vital role in processes such as iron metabolism, neurotransmitter synthesis, and antioxidant defense. Copper ions, particularly when released from intrauterine devices, have been shown to decrease sperm viability, thereby impacting fertility.

Pharmacokinetics

Copper is absorbed from the gut and is predominantly transported in the plasma bound to proteins such as ceruloplasmin and albumin. The absorption efficiency can vary; however, a significant portion of dietary copper is usually absorbed. The body regulates copper levels through hepatic excretion and storage mechanisms, ensuring homeostasis. Excess copper can lead to toxicity, while deficiency results in various health issues.

Pregnancy

Copper is considered essential during pregnancy, but excessive intake should be avoided due to potential toxicity.

Breast-feeding

Copper is excreted in breast milk, and adequate maternal intake is important for infant development.

Storage

Store in a cool, dry place, away from moisture and heat.

Indications

• Calcium deficiency
• Osteoporosis prevention
• Osteomalacia
• Rickets
• Dietary supplementation in individuals with increased calcium and phosphorus requirements

Dosage

Children: Refer to established guidelines for specific dosing based on clinical indications and individual patient needs.

Adults: Refer to established guidelines for specific dosing based on clinical indications and individual patient needs.

Mechanism of action

Dicalcium phosphate dissociates in the gastrointestinal tract to release calcium and phosphate ions. Calcium plays a vital role in various physiological processes, including muscle contraction, neurotransmitter release, and blood coagulation. The phosphate ions are essential for energy metabolism and are integral to the formation of ATP (adenosine triphosphate), nucleic acids, and cellular membranes. The availability of these ions supports bone mineralization and overall skeletal integrity.

Pharmacodynamics

The pharmacodynamics of dicalcium phosphate involves its role in maintaining calcium and phosphate homeostasis in the body. Adequate levels of calcium are critical for normal bone metabolism, while phosphate is necessary for the formation of hydroxyapatite in bone tissue. The balance of these minerals is regulated by hormones such as parathyroid hormone and calcitriol, which modulate their absorption in the intestines and reabsorption in the kidneys. Supplementation with dicalcium phosphate can help alleviate deficiencies and support bone health.

Pharmacokinetics

Dicalcium phosphate is absorbed in the gastrointestinal tract, with varying absorption rates depending on the presence of other dietary components. Calcium absorption occurs primarily in the small intestine, while phosphate absorption can occur throughout the gastrointestinal tract. After absorption, calcium is distributed to bones, teeth, and soft tissues, while excess calcium is excreted through urine. The pharmacokinetics may be influenced by factors such as age, dietary habits, and the presence of gastrointestinal disorders.

Adverse effects

• Gastrointestinal disturbances (nausea, constipation)
• Hypercalcemia
• Kidney stones
• Fatigue
• Muscle weakness

Interactions

• May interact with calcium channel blockers
• Increased risk of hypercalcemia with thiazide diuretics
• May affect the absorption of certain antibiotics (e.g., tetracyclines)

Precautions

• Use with caution in patients with renal impairment
• Monitor calcium levels in patients receiving high doses
• Consider potential interactions with other medications

Pregnancy

Dicalcium is generally considered safe in pregnancy when used as directed, but high doses should be avoided.

Breast-feeding

Calcium is an essential nutrient during breastfeeding, but excessive supplementation should be approached with caution.

Storage

Store in a cool, dry place, away from direct sunlight and moisture.

Formulations

• Tablets
• Powders
• Chewable tablets

Indications

• Calcium deficiency
• Magnesium deficiency
• Osteoporosis prevention
• Nutritional supplementation

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines based on age and weight.

Adults: Refer to the BNF for appropriate dosing guidelines based on specific conditions.

Mechanism of action

Dolomite acts as a source of calcium and magnesium, which are essential for various physiological processes. Calcium is critical for bone health, muscle function, and neurotransmission, while magnesium plays a vital role in muscle contraction, nerve function, and energy production.

Pharmacodynamics

The pharmacodynamic effects of dolomite are primarily attributed to its mineral content. Calcium and magnesium contribute to bone mineralization, help maintain normal heart rhythm, and are involved in enzymatic processes. The balance of these minerals is crucial for maintaining proper physiological function and preventing deficiencies.

Pharmacokinetics

Dolomite is absorbed in the gastrointestinal tract, where it dissociates into its constituent ions, calcium and magnesium. The absorption rates can vary based on the individual's digestive health and the presence of other dietary components. Once absorbed, calcium is primarily stored in bones and teeth, while magnesium is distributed throughout the body, especially in bones, muscles, and soft tissues. The excretion of excess calcium and magnesium occurs primarily through the kidneys.

Pregnancy

There is limited information regarding the use of dolomite during pregnancy. It is advisable to consult a healthcare professional before use.

Breast-feeding

There is limited information regarding the use of dolomite during breastfeeding. It is advisable to consult a healthcare professional before use.

Storage

Store in a cool, dry place, away from direct sunlight.

Indications

• Iodine deficiency
• Goiter
• Hypothyroidism
• Thyroiditis
• Fibrocystic breast disease

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines based on age and weight.

Adults: Refer to the BNF for appropriate dosing guidelines based on condition and clinical judgment.

Mechanism of action

Molecular iodine inhibits the induction and promotion of carcinogenesis in mammary tissues and has shown beneficial effects in fibrocystic breast disease. It temporarily decreases thyroid hormone production through the acute Wolff-Chaikoff effect, followed by a return to normal hormone synthesis due to down regulation of the sodium-iodide symport. This mechanism can lead to a transient hypothyroid state in some individuals with underlying thyroid conditions.

Pharmacodynamics

Iodine is vital for the synthesis of thyroid hormones thyroxine (T4) and triiodothyronine (T3). It affects the metabolism of amine-derived hormones and plays a role in amino acid metabolism. The acute excess of iodide can lead to decreased circulating levels of T4 and T3 in susceptible individuals, while most people can escape this effect and maintain normal thyroid function.

Pharmacokinetics

Iodine is absorbed primarily in the gastrointestinal tract and is distributed throughout the body, particularly in the thyroid gland, where it is concentrated for hormone synthesis. The kidney plays a significant role in the excretion of excess iodine. The half-life of iodine in the body varies and can be influenced by dietary intake and underlying health conditions.

Adverse effects

• Hypothyroidism
• Hyperthyroidism
• Iodine allergy
• Gastrointestinal disturbances

Interactions

• Thyroid hormones
• Antithyroid drugs
• Lithium
• Diuretics

Precautions

• Use with caution in patients with thyroid dysfunction
• Monitor thyroid function periodically during treatment
• Pregnant or breastfeeding women should consult a healthcare provider before use

Pregnancy

Iodine is essential for fetal thyroid hormone synthesis, but excessive iodine intake should be avoided.

Breast-feeding

Iodine is excreted in breast milk; consult a healthcare provider regarding supplementation.

Storage

Store in a cool, dry place away from light.

Formulations

• Iodine solution
• Iodine tincture
• Potassium iodide tablets

Dosage

Children: Refer to specific medication guidelines for appropriate dosing.

Adults: Refer to specific medication guidelines for appropriate dosing.

Pregnancy

The safety of irish during pregnancy has not been established. Use only if potential benefits justify the risks.

Breast-feeding

It is unknown whether irish is excreted in human milk. Caution is advised when using during breastfeeding.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Seasonal allergic rhinitis
• Perennial allergic rhinitis
• Chronic urticaria
• Asthma (adjunct therapy)

Dosage

Children: Refer to the BNF for Children for pediatric dosing guidelines.

Adults: Refer to the BNF for specific dosing recommendations.

Mechanism of action

Astemizole competes with histamine for binding at H1-receptor sites in the gastrointestinal tract, uterus, large blood vessels, and bronchial muscle. This reversible binding suppresses the formation of edema, flare, and pruritus resulting from histaminic activity. Astemizole does not readily cross the blood-brain barrier, leading to minimal central nervous system depression.

Pharmacodynamics

Astemizole is classified as a second-generation H1-receptor antagonist, designed to provide relief from allergic symptoms without significant sedation. Its pharmacodynamic properties allow it to effectively mitigate histamine-mediated conditions such as allergic rhinitis and urticaria, while causing minimal CNS effects due to its limited penetration of the blood-brain barrier.

Pharmacokinetics

Astemizole exhibits a remarkably long half-life of elimination, estimated to be between 12 to 18 days for its metabolites. This prolonged duration of action allows for less frequent dosing while maintaining therapeutic efficacy. Due to its peripheral binding characteristics, it avoids significant interactions with cholinergic receptors.

Pregnancy

Astemizole should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether astemizole is excreted in human milk. Caution is advised when administering to nursing mothers.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Tablets

Indications

• Anti-inflammatory effects
• Antimicrobial properties
• Wound healing
• Traditional herbal medicine applications

Dosage

Children: Refer to established herbal medicine guidelines or consult a healthcare professional for dosing information, as specific dosing regimens for moss are not standardized.

Adults: Refer to established herbal medicine guidelines or consult a healthcare professional for dosing information, as specific dosing regimens for moss are not standardized.

Mechanism of action

The mechanisms of action of moss components can vary significantly by species. Some mosses contain bioactive compounds such as flavonoids, terpenoids, and alkaloids, which may exert antioxidant activity, modulate inflammatory pathways, or promote cellular repair processes. These compounds can interact with various biological targets, including enzymes and receptors, leading to pharmacological effects.

Pharmacodynamics

Pharmacodynamics of moss-derived compounds may include effects such as inhibition of inflammatory mediators, modulation of immune responses, and promotion of wound healing through enhanced cellular regeneration. The specific pharmacodynamic properties are heavily dependent on the active compounds present in the moss species being studied.

Pharmacokinetics

The pharmacokinetics of moss compounds are not well characterized. However, it is generally understood that bioactive compounds from plants may undergo absorption in the gastrointestinal tract, followed by metabolism in the liver. The extent of absorption and metabolism, along with the half-life of these compounds, can vary widely based on the specific moss species and the form in which it is administered.

Pregnancy

The safety of moss during pregnancy has not been established. It is advisable to consult a healthcare provider before use.

Breast-feeding

The effects of moss on breastfeeding have not been thoroughly studied. Caution is recommended.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Malnutrition
• Postoperative recovery
• Protein deficiency
• Chronic illness
• Gastrointestinal absorption disorders

Dosage

Children: Refer to the specific product guidelines and clinical judgment for dosing, as it may vary based on individual needs and clinical conditions.

Adults: Refer to the specific product guidelines and clinical judgment for dosing, as it may vary based on individual needs and clinical conditions.

Mechanism of action

Peptonate works by providing readily absorbable amino acids that can be utilized for protein synthesis and various metabolic processes in the body. The peptones are broken down into smaller peptides and amino acids in the digestive system, which can then be easily absorbed into the bloodstream.

Pharmacodynamics

Peptonate enhances nutritional status by supplying essential and non-essential amino acids necessary for various physiological functions, including tissue repair, immune response, and hormone production. The presence of these amino acids in the bloodstream assists in anabolic processes and may improve overall metabolic functions in patients with compromised nutritional intake.

Pharmacokinetics

After administration, peptonate is digested in the gastrointestinal tract, where it is hydrolyzed into free amino acids and smaller peptides. These components are absorbed primarily in the small intestine and enter the systemic circulation. The bioavailability of amino acids from peptonate is high, as they are readily taken up by intestinal villi. The metabolism of amino acids occurs in the liver and other tissues, where they are utilized for protein synthesis or converted into energy substrates.

Pregnancy

Safety during pregnancy has not been established. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether peptonate is excreted in human milk. Caution should be exercised when administering to nursing mothers.

Storage

Store in a cool, dry place, away from direct sunlight. Keep out of reach of children.

Indications

• Hypophosphatemia
• Bone disorders (e.g., osteomalacia, rickets)
• Nutritional supplementation in deficiency states

Dosage

Children: Refer to BNF for Children for specific paediatric dosing guidance based on the condition being treated.

Adults: Refer to BNF for specific adult dosing guidance based on the condition being treated.

Mechanism of action

Phosphorus decreases the absorption of intercellular calcified cartilage matrix by osteoclasts in the metaphyseal region of growing bones, leading to increased bone density and thickness, observable as 'phosphorus bands' on radiographs. Additionally, exposure to white phosphorus damages the rough and smooth endoplasmic reticulum, impairing protein synthesis and lipid transport, particularly affecting the synthesis of very low-density lipoproteins (VLDL) and causing hepatic steatosis and fibrosis.

Pharmacodynamics

Phosphorus is involved in bone metabolism and energy transfer within cells. It contributes to the structural framework of bones and teeth, and its role in ATP formation is crucial for energy metabolism. The balance of phosphorus with calcium and vitamin D is essential for maintaining bone health and preventing disorders such as osteomalacia and rickets.

Pharmacokinetics

Phosphorus is absorbed in the gastrointestinal tract, with absorption rates affected by factors such as dietary composition and the presence of other minerals. It is distributed throughout body tissues, particularly in bones and teeth. Phosphorus is primarily excreted through the kidneys, and its serum levels are regulated by hormonal influences, including parathyroid hormone and calcitriol.

Pregnancy

Phosphorus is essential for fetal development; however, excessive intake should be avoided. Consult healthcare professionals for appropriate supplementation.

Breast-feeding

Phosphorus is secreted in breast milk; adequate maternal intake is important for infant health. Consult healthcare professionals for guidance.

Storage

Store in a cool, dry place, away from direct sunlight and moisture. Ensure it is kept out of reach of children.

Indications

• Calcium deficiency
• Osteoporosis prevention and treatment
• Hypoparathyroidism
• Rickets
• Paget's disease of bone
• Muscle spasms
• Pregnancy and lactation-related calcium supplementation

Dosage

Children: Refer to BNF for Children for specific dosing recommendations based on age and condition.

Adults: Refer to BNF for specific dosing recommendations based on condition and formulation.

Mechanism of action

Tricalcium acts by increasing the availability of calcium ions in the bloodstream. Calcium is critical for several biological processes, including the maintenance of bone structure and function, muscle contraction, neurotransmitter release, and blood clotting. It plays a pivotal role in the cellular signaling pathways that regulate these functions.

Pharmacodynamics

Calcium is essential for the formation and maintenance of bone tissue. It contributes to bone mineralization and is a key component in the architecture of bones. Calcium also affects the function of various enzymes and hormones, modulating processes such as nerve impulse transmission and muscle contraction. The balance of calcium ions is maintained through a complex interaction between dietary intake, renal excretion, and hormonal regulation (primarily involving parathyroid hormone and vitamin D).

Pharmacokinetics

Calcium absorption occurs primarily in the small intestine, with the efficiency influenced by dietary factors, age, and the presence of other nutrients. Once absorbed, calcium is distributed in the body, with approximately 99% stored in bones and teeth. The remaining 1% circulates in the blood and is involved in physiological functions. Calcium levels are tightly regulated through intestinal absorption, renal excretion, and the release of calcium from bone stores, maintaining a serum calcium concentration within a narrow range.

Contra-indications

• Hypercalcemia
• Severe renal impairment
• Hyperparathyroidism

Adverse effects

• Constipation
• Nausea
• Vomiting
• Abdominal pain
• Kidney stones
• Hypercalcemia symptoms (e.g., confusion, muscle weakness)

Interactions

• Calcium supplements may decrease the absorption of certain medications like bisphosphonates and tetracyclines.
• Thiazide diuretics may increase the risk of hypercalcemia.

Precautions

• Use with caution in patients with renal impairment.
• Monitor calcium levels in patients receiving chronic therapy.
• Assess dietary calcium intake to avoid excessive supplementation.

Pregnancy

Tricalcium is generally considered safe during pregnancy, but should be used under medical supervision to avoid exceeding recommended dietary allowances.

Breast-feeding

Calcium supplementation is compatible with breastfeeding, but it is advisable to consult a healthcare provider regarding appropriate dosing.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Tablets
• Chewable tablets
• Powder for oral solution
• Effervescent tablets

Indications

• Nutritional supplement
• Antioxidant support
• Anti-inflammatory support
• Potential cancer prevention

Dosage

Children: Refer to established dietary recommendations, as specific dosing is not defined in the BNF.

Adults: Refer to established dietary recommendations, as specific dosing is not defined in the BNF.

Mechanism of action

Watercress contains glucosinolates, which are sulfur-containing compounds that can be converted into biologically active forms, such as isothiocyanates. These compounds are believed to exert protective effects against cancer by modulating detoxification enzymes and influencing cell signaling pathways related to inflammation and apoptosis.

Pharmacodynamics

The pharmacodynamic effects of watercress are primarily attributed to its bioactive compounds, including flavonoids, glucosinolates, and vitamins. These agents contribute to the anti-inflammatory and antioxidant effects of watercress, potentially reducing the risk of chronic diseases and promoting overall health. The presence of vitamin K plays a crucial role in blood coagulation, while vitamins A and C support immune function.

Pharmacokinetics

The pharmacokinetics of watercress are not extensively studied due to its classification as a food rather than a pharmaceutical agent. However, the absorption and bioavailability of its phytochemicals may vary based on preparation methods and individual metabolism. Generally, the compounds in watercress are readily absorbed when consumed, contributing to their physiological effects.

Pregnancy

Watercress is generally considered safe to eat during pregnancy in moderation, but excessive consumption should be avoided due to potential high nitrate levels.

Breast-feeding

Watercress is safe to consume during breastfeeding in moderate amounts. However, excessive intake should be avoided.

Storage

Store in a cool, dry place. Fresh watercress should be kept in the refrigerator and consumed within a few days of purchase.

Formulations

• Fresh watercress (whole leaves)
• Watercress juice
• Dried watercress supplements

Mechanism of action

Copper is absorbed from the gut via high affinity copper uptake protein and likely through low affinity copper uptake protein and natural resistance-associated macrophage protein-2. It is believed that copper is reduced to the Cu1+ form prior to transport. Once inside the enterocyte, it is bound to copper transport protein ATOX1 which shuttles the ion to copper transporting ATPase-1 on the golgi membrane which take up copper into the golgi apparatus. Once copper has been secreted by enterocytes into the systemic circulation it remain largely bound by ceruloplasmin (65-90%), albumin (18%), and alpha 2-macroglobulin (12%). Copper is an essential element in the body and is incorporated into many oxidase enzymes as a cofactor. It is also a component of zinc/copper super oxide dismutase, giving it an anti-oxidant role. Copper defiency occurs in Occipital Horn Syndrome and Menke's disease both of which are associated with impaired development of connective tissue due to the lack of copper to act as a cofactor in protein-lysine-6-oxidase. Menke's disease is also associated with progressive neurological impairment leading to death in infancy. The precise mechanisms of the effects of copper deficiency are vague due to the wide range of enzymes which use the ion as a cofactor. Copper appears to reduce the viabilty and motility of spermatozoa. This reduces the likelihood of fertilization with a copper IUD, producing copper's contraceptive effect. The exact mechanism of copper's effect on sperm are unknown. The reason for the less severe reaction when the foreign body is at a distance from the retina has been proposed to be ... that near the retina & its blood vessels there is greater oxygen tension than at a distance, which causes metallic copper to oxidize to toxic copper compounds more rapidly close to or in contact with the retina than at a distance. Furthermore, the abscess formation that is characteristic of copper undergoing oxidation close to the retina & choroiod can be attributed to attraction of polymorphonuclear leukocytes from these nearby vascular tissues, which become heavily infiltrated. Liquefaction & disorganization of the vitreous body has been explained on the basis of copper catalysis of oxidation of ascorbic acid, leading to depolymerization of the hyaluronic acid of the vitreous humor. Changes in protein & hexosamine content have also been related to decrease in viscosity of the vitreous humor. Increased content of amino acids in the vitreous humor has been consistent with proteolysis of the vitreous body, but decreased concentration in the aqueous humor has suggested suppression of secretion of amino acids by the ciliary body under the influence of copper.

Pharmacodynamics

Copper is incorporated into many enzymes throughout the body as an essential part of their function. Copper ions are known to reduce fertility when released from copper-containing IUDs.

Mechanism of action

Molecular iodine is known to inhibit the induction and promotion of N-methyl-n-nitrosourea-induced mammary carcinogenesis, to regress 7,12-dimethylbenz(a)anthracene-induced breast tumors in rats.It has also been shown to have beneficial effects in fibrocystic human breast disease. An acute iodide excess (above the preexisting dietary intake) transiently decreases the production of thyroid hormones in the thyroid gland; this is referred to as the acute Wolff-Chaikoff effect. In normal people, this is followed by a return to normal levels of hormone synthesis, referred to as escape from the acute Wolff-Chaikoff effect, without a significant change in circulating hormone levels. Escape is thought to be the result of down regulation of the sodium-iodide symport (NIS), the iodide transporter in the thyroid gland, resulting in a decrease in the intrathyroidal iodine and the resumption of normal hormone synthesis. An acute or chronic excess of iodide can also decrease circulating T4 and T3 levels and induce a hypothyroid state in some people who have underlying thyroid disorders. These effects are the result of a failure to escape from the acute Wolff-Chaikoff effect. Most people who experience iodine-induced hypothyroidism recover when the excess iodine intake is discontinued.

Mechanism of action

Astemizole competes with histamine for binding at H₁-receptor sites in the GI tract, uterus, large blood vessels, and bronchial muscle. This reversible binding of astemizole to H₁-receptors suppresses the formation of edema, flare, and pruritus resulting from histaminic activity. As the drug does not readily cross the blood-brain barrier and preferentially binds at H1 receptors in the peripehery rather than within the brain, CNS depression is minimal. Astemizole may also act on H₃-receptors, producing adverse effects. Antihistamines are effective therapy against histamine-mediated conditions, including seasonal and perennial allergic rhinitis and chronic urticaria. They may also have a therapeutic role to play in asthma. Until recently all antihistamines produced some degree of drowsiness, as well as having anticholinergic side effects. Several non-sedating antihistamines have now been developed. Evidence suggests that their freedom from central nervous system effects is due to their lack of penetration of the blood brain barrier. They also have no appreciable binding to cholinergic receptors. Two of these non-sedating antihistamines, terfenadine and astemizole, have novel binding characteristics with the histamine H1 receptor, exhibiting irreversible binding at higher concentrations. In humans astemizole has a remarkably long half-life of elimination, on the order of 12 to 18 days for metabolites. Clinical trials have demonstrated that these newer antihistamines are as effective as classical antihistamines and that they have no greater incidence of central nervous system or anticholinergic side effects than placebo. QT interval prolongation and torsade de pointes are associated with astemizole intake and have been ascribed to block the repolarizing K+ currents, specifically the rapidly activating component of the delayed rectifier iKr. ... The perforated patch clamp recording technique was used to study the effects of desmethylastemizole (20 nmol/liter) on action potentials and iKr in isolated rabbit ventricular myocytes. Desmethylastemizole produced action potential prolongation and the induction of plateau early afterdepolarizations. Under voltage clamp conditions, desmethylastemizole suppressed iKr amplitude by approximately 65%. The drug E-4031 (100 nmol/liter), which selectively blocks iKr, had a similar effect on current amplitude. Desmethylastemizole, the major astemizole metabolite, blocks the repolarizing K+ current iKr with high affinity. The clinical observation of QT prolongation and torsade de pointes found with astemizole intake may principally be caused by the proarrhythmic effects of its metabolite desmethylastemizole. Astemizole /has/ been recognized in rare cases to induce the syndrome of torsades de pointes, i.e. QT interval prolongation and life-threatening ventricular tachycardia. /It/ was found to prolong cardiac repolarization when its metabolic elimination was impaired, such as by liver disease or drugs that inhibit the 3A family of cytochrome P450. In vitro studies indicate that this action is due to blockade of one or more of the cardiac potassium channels that determine the duration of the action potential.

Pharmacodynamics

Astemizole is a second generation H₁-receptor antagonist. It does not significantly cross the blood brain barrier and therefore does not cause drowsiness or CNS depression at normal doses.

Mechanism of action

Phosphorus apparently decreases the absorption of intercellular calcified cartilage matrix by osteoclasts, in the metaphyseal region of growing bones. Administration of phosphorus to growing animals or children produces "phosphorus bands" of increased bone density and thickness that are visible grossly or from radiograms. The "phosphorus bands" are observed in the metaphyseal region of growing bones, and represent areas of decreased absorption of the calcified cartilage matrix. Exposure to white phosphorus has been shown to damage the rough endoplasmic reticulum and cause a disaggregation of polyribosomes. This damage results in impairment of protein synthesis, in particular, a decrease in the synthesis of the apolipoprotein portion of very low density lipoproteins (VLDL), which are required for the transport of triglycerides. A significant decrease in protein synthesis has been detected as early as 3 hours after oral exposure. The smooth endoplasmic reticulum is also involved in the formation of the VLDLs, and damage to the smooth endoplasmic reticulum also impairs the formation of VLDLs. The net result of these ultrastructural changes is an accumulation of triglycerides in the liver. This results in steatosis and fibrosis, which is one of the mechanisms involved in the hepatotoxicity of white phosphorus. The mechanism behind the damage to the endoplasmic reticulum is not known; also, it is not known whether white phosphorus itself or a metabolite of white phosphorus is the damaging agent. In addition to these damages, white phosphorus or a metabolite causes damage to the mitochondria and nuclei in the livers of animals orally exposed to white phosphorus. The damage to the mitochondria may impair the cell's ability to produce ATP, thus resulting in necrosis of the cell. Fatty infiltration and/or cellular damage has also been observed in the kidney, brain, and heart. It is possible that white phosphorus (or a metabolite) also impairs the ability of cells in these organs to produce ATP. The mitochondrial damage may also inhibit fatty acid oxidation (also contributing to the decreased availability of ATP) which could result in an accumulation of fat in the organs.